Diuretics — MCQs
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An 82-year-old man with congestive heart failure and a creatinine clearance (CrCl) of 17 mL/min requires a diuretic for the treatment of peripheral edema. Which of the following diuretics would be most appropriate in this patient?
Which of the following drugs causes osmotic diuresis?
Which is a safe diuretic in renal dysfunction?
A 72-year-old woman with mild heart failure is treated overzealously with a thiazide diuretic. A few days later, the woman complains of muscle weakness, and laboratory tests demonstrate hypokalemia. Which of the following is most likely increased in this woman?
A 55-year-old man with congestive heart failure is noted to be taking furosemide each day. Which of the following is most likely to be found in the serum?
Furosemide acts by inhibiting which of the following?
Which of the following statements about diuretics is NOT true?
All of the following diuretics inhibit the Na+-K+-2Cl- symporter, except?
Furosemide is useful in:
Hyperkalemia is caused by all EXCEPT:
Diuretics Indian Medical PG Practice Questions and MCQs
Question 21: An 82-year-old man with congestive heart failure and a creatinine clearance (CrCl) of 17 mL/min requires a diuretic for the treatment of peripheral edema. Which of the following diuretics would be most appropriate in this patient?
- A. Furosemide (Correct Answer)
- B. Hydrochlorothiazide
- C. Indapamide
- D. Spironolactone
Explanation: ### Explanation **1. Why Furosemide is Correct:** The patient has severe renal impairment (CrCl 17 mL/min). In patients with a **Creatinine Clearance (CrCl) < 30 mL/min**, thiazide diuretics lose their efficacy because they cannot reach the site of action (the distal convoluted tubule) in sufficient concentrations. **Loop diuretics**, such as **Furosemide**, remain effective even at low GFR/CrCl levels. They are the drugs of choice for managing volume overload in patients with advanced chronic kidney disease (CKD) or congestive heart failure with renal impairment. **2. Why the Other Options are Incorrect:** * **Hydrochlorothiazide:** This is a thiazide diuretic. As a general rule for NEET-PG, thiazides are ineffective when the **GFR is < 30 mL/min**. They fail to produce significant diuresis in patients with severe renal insufficiency. * **Indapamide:** Although it is a thiazide-like diuretic often used in hypertension, it also loses its diuretic efficacy in severe renal failure (CrCl < 30 mL/min). * **Spironolactone:** This is a potassium-sparing diuretic. It is generally **contraindicated** or used with extreme caution in patients with severe renal impairment (CrCl < 30 mL/min) due to the high risk of life-threatening **hyperkalemia**. **3. High-Yield Clinical Pearls for NEET-PG:** * **Site of Action:** Loop diuretics act on the thick ascending limb of the Loop of Henle (inhibiting Na⁺-K⁺-2Cl⁻ cotransporter). * **Metolazone Exception:** Most thiazides fail at CrCl < 30 mL/min, but **Metolazone** (a thiazide-like diuretic) is a notable exception that can still work in renal failure, often used in combination with loop diuretics to overcome "diuretic resistance." * **Ototoxicity:** Furosemide can cause dose-dependent ototoxicity, especially when given intravenously at high doses or combined with aminoglycosides. * **Electrolyte Changes:** Loop diuretics cause "Low everything" (Hypokalemia, Hypomagnesemia, Hypocalcemia), whereas Thiazides cause **Hypercalcemia**.
Question 22: Which of the following drugs causes osmotic diuresis?
- A. Mannitol
- B. Isosorbide
- C. Glycerol
- D. All of the above (Correct Answer)
Explanation: ### Explanation **Concept:** Osmotic diuretics are pharmacologically inert substances that are freely filtered at the glomerulus but undergo limited or no reabsorption by the renal tubules. They increase the osmolarity of the tubular fluid, creating an osmotic gradient that retains water within the lumen, thereby increasing urine volume. **Analysis of Options:** * **Mannitol:** The most commonly used osmotic diuretic. It is administered intravenously and is the drug of choice for reducing intracranial pressure (cerebral edema) and intraocular pressure. * **Isosorbide:** This is a polyhydric alcohol (not to be confused with the vasodilator Isosorbide dinitrate) that can be administered orally to reduce intraocular pressure in glaucoma. * **Glycerol (Glycerin):** Administered orally, it is rapidly absorbed and increases plasma osmolarity. It is frequently used to provide a rapid reduction in intraocular pressure before ophthalmic surgery. Since all three agents function by increasing the osmotic pressure of the glomerular filtrate to inhibit water reabsorption, **Option D (All of the above)** is correct. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Action:** Primarily the **Loop of Henle** (descending limb) and the **Proximal Convoluted Tubule (PCT)**. * **Contraindications:** Osmotic diuretics are strictly contraindicated in **Acute Pulmonary Edema** and **Congestive Heart Failure** because they initially expand the extracellular fluid (ECF) volume before diuresis occurs. They are also contraindicated in **Anuria** due to chronic renal failure. * **Therapeutic Uses:** Mannitol is used to maintain urine flow in acute renal failure (incipient stage) and to treat dialysis disequilibrium syndrome. * **Side Effect:** Headache, nausea, and vomiting are common; hyponatremia may occur initially, followed by dehydration and hypernatremia.
Question 23: Which is a safe diuretic in renal dysfunction?
- A. Mannitol
- B. Bumetanide (Correct Answer)
- C. Chlorthalidone
- D. Acetazolamide
Explanation: ### Explanation **Correct Answer: B. Bumetanide** **Why Bumetanide is the correct choice:** Bumetanide is a high-ceiling **Loop Diuretic**. Loop diuretics (including Furosemide and Torsemide) are the diuretics of choice in patients with renal dysfunction (GFR < 30 ml/min). Unlike other classes, loop diuretics maintain their efficacy even when the glomerular filtration rate (GFR) is significantly reduced. They act on the thick ascending limb of the Loop of Henle, which has a large capacity for sodium reabsorption, ensuring a potent natriuretic effect even in failing kidneys. **Why the other options are incorrect:** * **Mannitol (Osmotic Diuretic):** It is contraindicated in established anuria or severe renal failure. It expands extracellular fluid volume, which can lead to acute pulmonary edema and heart failure in patients who cannot excrete the fluid load. * **Chlorthalidone (Thiazide-like Diuretic):** Thiazides and related drugs generally lose their efficacy when the GFR falls below 30 ml/min (with the exception of Metolazone). They are not the preferred agents for fluid management in advanced renal impairment. * **Acetazolamide (Carbonic Anhydrase Inhibitor):** It is a weak diuretic that acts on the proximal tubule. It is avoided in renal failure as it can worsen metabolic acidosis (a common complication of uremia) and has a very limited diuretic effect. **High-Yield Clinical Pearls for NEET-PG:** * **Potency Ratio:** Bumetanide is roughly **40 times more potent** than Furosemide (1 mg Bumetanide ≈ 40 mg Furosemide). * **Metolazone Exception:** While most thiazides fail in renal impairment, **Metolazone** remains effective and is often combined with loop diuretics to overcome "diuretic resistance" (Sequential Nephron Blockade). * **Ototoxicity:** While all loop diuretics can cause ototoxicity, **Ethacrynic acid** is the most ototoxic, while Bumetanide is generally considered to have a lower risk compared to high-dose Furosemide.
Question 24: A 72-year-old woman with mild heart failure is treated overzealously with a thiazide diuretic. A few days later, the woman complains of muscle weakness, and laboratory tests demonstrate hypokalemia. Which of the following is most likely increased in this woman?
- A. Serum H+ concentration
- B. Plasma aldosterone (Correct Answer)
- C. Plasma sodium
- D. Potassium retention
Explanation: **Explanation:** The correct answer is **B. Plasma aldosterone**. **Mechanism of Action:** Thiazide diuretics inhibit the $Na^+/Cl^-$ symporter in the distal convoluted tubule, leading to increased excretion of sodium and water. Overzealous use causes **volume depletion** (hypovolemia). This reduction in effective circulating volume triggers the **Renin-Angiotensin-Aldosterone System (RAAS)**. Juxtaglomerular cells sense decreased renal perfusion and release renin, ultimately leading to elevated levels of **Aldosterone**. Aldosterone then acts on the collecting ducts to reabsorb sodium at the expense of secreting potassium and hydrogen ions, which explains the patient's hypokalemia and muscle weakness. **Analysis of Incorrect Options:** * **A. Serum $H^+$ concentration:** Thiazides cause **metabolic alkalosis** (contraction alkalosis and increased $H^+$ secretion in the collecting duct). Therefore, $H^+$ concentration decreases, and pH increases. * **C. Plasma sodium:** Thiazides are a common cause of **hyponatremia**. They promote sodium excretion while the compensatory ADH release (due to volume depletion) causes water retention, diluting serum sodium. * **D. Potassium retention:** Thiazides cause **potassium wasting** (hypokalemia) due to increased sodium delivery to the late distal tubule and high aldosterone levels, both of which drive $K^+$ secretion. **NEET-PG High-Yield Pearls:** * **Thiazide Side Effects (Hyper-GLUC):** Hyper**G**lycemia, Hyper**L**ipidemia, Hyper**U**ricemia, and Hyper**C**alcemia. * **Electrolyte Profile:** Hypokalemic metabolic alkalosis + Hyponatremia. * **Clinical Note:** Unlike Loop diuretics (which cause hypocalcemia), Thiazides decrease urinary calcium and are used in treating **calcium nephrolithiasis**.
Question 25: A 55-year-old man with congestive heart failure is noted to be taking furosemide each day. Which of the following is most likely to be found in the serum?
- A. Decreased uric acid level
- B. Low bicarbonate level
- C. Decreased potassium level (Correct Answer)
- D. Elevated magnesium level
Explanation: **Explanation:** **Mechanism of Action (The Correct Answer):** Furosemide is a high-ceiling **loop diuretic** that inhibits the **Na+/K+/2Cl- symporter** in the Thick Ascending Limb (TAL) of the Henle’s loop. By blocking this transporter, it increases the delivery of sodium to the distal convoluted tubule and collecting duct. In the collecting duct, the increased sodium load promotes sodium reabsorption in exchange for **potassium (K+) and hydrogen (H+) ions** via the action of aldosterone. This leads to increased urinary excretion of potassium, resulting in **hypokalemia** (decreased serum potassium levels). **Analysis of Incorrect Options:** * **A. Decreased uric acid level:** Incorrect. Loop diuretics cause **hyperuricemia** (elevated uric acid). This occurs because diuretics cause volume depletion, leading to increased proximal tubular reabsorption of uric acid, and they compete with uric acid for the organic acid secretory pathway in the kidney. * **B. Low bicarbonate level:** Incorrect. Furosemide causes **contraction alkalosis**, which is characterized by an **increase** in serum bicarbonate levels due to the loss of H+ ions and volume contraction. * **D. Elevated magnesium level:** Incorrect. The Na+/K+/2Cl- symporter normally creates a positive lumen potential that drives the paracellular reabsorption of divalent cations. By inhibiting this, furosemide causes **hypomagnesemia** and **hypocalcemia**. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Loop Diuretic Side Effects:** "OH DANG!" (**O**totoxicity, **H**ypokalemia, **D**ehydration, **A**llergy (sulfa), **N**ephritis, **G**out). * **Calcium Handling:** Unlike Thiazides (which cause hypercalcemia), Loop diuretics cause **hypocalcemia** ("Loops Lose Calcium"). * **Drug of Choice:** Furosemide is the drug of choice for acute pulmonary edema in CHF due to its rapid-acting diuretic and vasodilator properties.
Question 26: Furosemide acts by inhibiting which of the following?
- A. Na+-K+-2Cl- cotransporter (Correct Answer)
- B. Na+-Cl- cotransporter
- C. Carbonic anhydrase
- D. Epithelial Na+ channels
Explanation: ### Explanation **Correct Option: A. Na+-K+-2Cl- cotransporter (NKCC2)** Furosemide is a potent **Loop Diuretic**. It acts on the **thick ascending limb (TAL)** of the Henle’s loop, which is responsible for reabsorbing approximately 25% of filtered sodium. Furosemide binds to the Cl⁻ binding site of the **Na⁺-K⁺-2Cl⁻ symporter (NKCC2)** on the luminal membrane, inhibiting the reabsorption of these electrolytes. This leads to a massive loss of Na⁺, Cl⁻, and water in the urine. **Analysis of Incorrect Options:** * **B. Na⁺-Cl⁻ cotransporter:** This is the target of **Thiazide diuretics** (e.g., Hydrochlorothiazide) acting on the **Distal Convoluted Tubule (DCT)**. * **C. Carbonic anhydrase:** This enzyme is inhibited by **Acetazolamide** in the **Proximal Convoluted Tubule (PCT)**, leading to bicarbonate loss. * **D. Epithelial Na⁺ channels (ENaC):** These channels are blocked by **Potassium-sparing diuretics** like **Amiloride** and **Triamterene** in the late distal tubule and collecting duct. **High-Yield Clinical Pearls for NEET-PG:** 1. **Site of Action:** Thick Ascending Limb (TAL) – often called "High-ceiling diuretics" due to their high efficacy. 2. **Electrolyte Changes:** Causes **Hypokalemia**, **Hypomagnesemia**, and **Hypocalcemia** (unlike Thiazides, which cause hypercalcemia). "Loops lose calcium." 3. **Ototoxicity:** A unique side effect, especially when used with aminoglycosides or in renal failure. 4. **Drug of Choice:** Acute Pulmonary Edema (due to rapid vasodilator action before the diuretic effect kicks in). 5. **Sulfa Allergy:** Furosemide is a sulfonamide derivative; caution is advised in patients with severe sulfa allergies (Ethacrynic acid is the alternative).
Question 27: Which of the following statements about diuretics is NOT true?
- A. Acetazolamide is a carbonic anhydrase stimulant. (Correct Answer)
- B. Thiazides act on the cortical diluting segment of the nephron.
- C. Furosemide is a high-ceiling diuretic.
- D. Spironolactone is an aldosterone antagonist.
Explanation: ### Explanation **1. Why Option A is the Correct Answer (The "Not True" Statement):** Acetazolamide is a **Carbonic Anhydrase (CA) Inhibitor**, not a stimulant. It works in the proximal convoluted tubule (PCT) by inhibiting the enzyme carbonic anhydrase. This prevents the dehydration of carbonic acid and the reabsorption of bicarbonate ($HCO_3^-$), leading to alkaline diuresis. Because it inhibits the enzyme, the statement claiming it is a "stimulant" is factually incorrect. **2. Analysis of Other Options:** * **Option B (Thiazides):** This is **true**. Thiazides act on the early distal convoluted tubule (DCT), which is also known as the **cortical diluting segment**. They inhibit the $Na^+-Cl^-$ symporter. * **Option C (Furosemide):** This is **true**. Furosemide is a loop diuretic that acts on the thick ascending limb of Henle. It is called "high-ceiling" because it has a steep dose-response curve, meaning increasing the dose leads to a proportional increase in diuresis over a wide range. * **Option D (Spironolactone):** This is **true**. It is a potassium-sparing diuretic that competitively inhibits the **aldosterone receptor** (Mineralocorticoid receptor) in the late DCT and collecting ducts. **3. NEET-PG High-Yield Clinical Pearls:** * **Acetazolamide Uses:** Glaucoma (decreases aqueous humor), Mountain sickness (induces metabolic acidosis to stimulate respiration), and Urinary alkalization. * **Side Effects:** Metabolic acidosis, hypokalemia, and sulfonamide-like hypersensitivity. * **Thiazide Paradox:** While they are diuretics, they are used to treat **Diabetes Insipidus** because they reduce glomerular filtration and increase proximal salt/water reabsorption. * **Furosemide Side Effects:** Remember the mnemonic **OH DANG**: **O**totoxicity, **H**ypokalemia, **D**ehydration, **A**llergy (sulfa), **N**ephritis, **G**out (hyperuricemia).
Question 28: All of the following diuretics inhibit the Na+-K+-2Cl- symporter, except?
- A. Furosemide
- B. Thiazide (Correct Answer)
- C. Ethacrynic acid
- D. Mersalyl
Explanation: The question tests the knowledge of the site of action and molecular targets of various diuretics. 1. Why Thiazide is the Correct Answer: Thiazide diuretics (e.g., Hydrochlorothiazide, Chlorthalidone) act on the **Distal Convoluted Tubule (DCT)** [1]. Their primary mechanism is the inhibition of the **Na+-Cl- symporter** (NCC) on the luminal membrane [1, 3]. They do not affect the Na+-K+-2Cl- (NKCC2) transporter [3]. 2. Analysis of Incorrect Options (Loop Diuretics): The other three options belong to the class of **Loop Diuretics**, which specifically inhibit the **Na+-K+-2Cl- (NKCC2) symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle [2, 4]: * **Furosemide:** A prototype high-ceiling loop diuretic (Sulfonamide derivative). * **Ethacrynic acid:** A phenoxyacetic acid derivative. It is a non-sulfonamide loop diuretic, making it the drug of choice for patients with sulfonamide allergies. * **Mersalyl:** An older organomercurial diuretic that also acts on the TAL to inhibit the same symporter, though it is now obsolete due to toxicity. Clinical Pearls for NEET-PG: * **Site of Action:** Loop diuretics act on the TAL (medullary and cortical), while Thiazides act on the cortical DCT. * **Calcium Handling:** This is a high-yield differentiator. Loop diuretics cause **Hypercalciuria** (used in treating hypercalcemia), whereas Thiazides cause **Hypocalciuria** (used in treating calcium nephrolithiasis). * **Ototoxicity:** Ethacrynic acid is the most ototoxic loop diuretic. * **Metabolic Side Effects:** Both classes can cause hypokalemia and metabolic alkalosis.
Question 29: Furosemide is useful in:
- A. Hypertension.
- B. Refractory oedema. (Correct Answer)
- C. Hypocalcemia.
- D. Hypokalemia.
Explanation: **Explanation:** **1. Why "Refractory Oedema" is correct:** Furosemide is a potent **Loop Diuretic** that acts by inhibiting the **Na⁺-K⁺-2Cl⁻ symporter** in the Thick Ascending Limb (TAL) of the Loop of Henle. It is known as a "high-ceiling" diuretic because it has a steep dose-response curve; increasing the dose leads to a progressive increase in diuresis. This makes it the drug of choice for **refractory oedema** (oedema not responding to milder diuretics) associated with Congestive Heart Failure, Nephrotic Syndrome, and Chronic Renal Failure. **2. Why other options are incorrect:** * **A. Hypertension:** While loop diuretics can be used in hypertension complicated by renal failure, **Thiazides** are the first-line diuretic for essential hypertension due to their longer duration of action and vasodilator properties. * **C. Hypocalcemia:** Furosemide increases the urinary excretion of calcium ("Loop loses Calcium"). Therefore, it is used to treat **Hypercalcemia**, not hypocalcemia. * **D. Hypokalemia:** Furosemide causes significant potassium loss in the urine. It is a *cause* of hypokalemia, not a treatment for it. **3. High-Yield NEET-PG Pearls:** * **Mechanism:** Inhibits Na⁺-K⁺-2Cl⁻ (NKCC2) in the TAL. * **Electrolyte Profile:** Causes Hypokalemia, Hypomagnesemia, and **Hypocalcemia**. * **Ototoxicity:** This is a unique side effect of loop diuretics, especially when used with aminoglycosides. * **Acute Pulmonary Oedema:** Furosemide is the drug of choice here, not just for its diuretic effect, but for its rapid **venodilatory action** (mediated by prostaglandins), which reduces cardiac preload.
Question 30: Hyperkalemia is caused by all EXCEPT:
- A. Loop diuretics (Correct Answer)
- B. Valsartan
- C. Amiloride
- D. Enalapril
Explanation: ### Explanation The correct answer is **Loop diuretics** because they cause **hypokalemia** (low potassium), not hyperkalemia. #### 1. Why Loop Diuretics (Option A) are the Correct Answer: Loop diuretics (e.g., Furosemide) inhibit the **Na⁺-K⁺-2Cl⁻ symporter** in the Thick Ascending Limb of the Loop of Henle. This leads to a massive delivery of sodium to the distal tubule. To reabsorb this sodium, the distal tubule activates the Na⁺/K⁺ exchange mechanism (driven by aldosterone), which results in the **excretion of potassium** into the urine. This process, combined with volume depletion-induced secondary hyperaldosteronism, leads to hypokalemia. #### 2. Why the other options are incorrect (They cause Hyperkalemia): * **Amiloride (Option C):** This is a potassium-sparing diuretic that blocks the **ENaC (Epithelial Sodium Channels)** in the collecting duct. By preventing sodium reabsorption, it reduces the negative luminal potential, thereby inhibiting the secretion of potassium into the lumen. * **Enalapril (Option D) & Valsartan (Option B):** Enalapril (an ACE inhibitor) and Valsartan (an ARB) both interfere with the **Renin-Angiotensin-Aldosterone System (RAAS)**. By decreasing aldosterone levels or blocking its action, they prevent potassium excretion in the distal nephron, leading to potassium retention. #### 3. NEET-PG High-Yield Pearls: * **Diuretics causing Hypokalemia:** Loop diuretics and Thiazides. * **Diuretics causing Hyperkalemia:** Spironolactone, Eplerenone (Aldosterone antagonists), Amiloride, and Triamterene. * **Clinical Tip:** Always monitor serum potassium when combining ACE inhibitors with potassium-sparing diuretics, as this significantly increases the risk of life-threatening hyperkalemia. * **ECG in Hyperkalemia:** Look for "Tall tented T-waves" and "Widened QRS complex."
Practice by Chapter
Carbonic Anhydrase Inhibitors
Practice Questions
Loop Diuretics
Practice Questions
Thiazide and Thiazide-Like Diuretics
Practice Questions
Potassium-Sparing Diuretics
Practice Questions
Carbonic Anhydrase Inhibitors
Practice Questions
Osmotic Diuretics
Practice Questions
Combination Diuretic Therapy
Practice Questions
Diuretics in Heart Failure
Practice Questions
Diuretics in Hypertension
Practice Questions
Diuretics in Renal Disorders
Practice Questions
Adverse Effects and Drug Interactions
Practice Questions
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